Biomedical subjects

W Derave

Publications and source records attributed to W Derave.

16 recordsLinked to original sources

PubMed2002

Treadmill exercise negatively affects visual contribution to static postural stability.

This study was undertaken to explore the nature of impaired postural stability following physical exercise. Nine healthy subjects (aged 24 +/- 3 years) were subjected to 30 min of treadmill walking or running on two separate occasions. Walking and running speeds (1.9 to 2.2 m/s) were chosen to induce equal energy expenditure. During treadmill exercise, kinematic analysis of head movement was performed. Prior to and immediately following exercise, postural sway was evaluated as mean velocity of centre of pressure (VCOP), measured on a force plate during 30 s quiet stance with eyes open or eyes closed. The results indicate that exercise increased two-dimensional postural sway by 9 - 19 % in eyes open, but not in the eyes closed condition. The deteriorating effect of exercise was both evident in the sagittal and in the frontal plane, although the effect on the former was slightly more transient. Post-exercise sway values were significantly higher after running than after walking. Kinematic analysis of head movement confirmed larger vertical displacement and acceleration pattern in running compared to walking. It is concluded that exercise of moderate intensity deteriorates visual contribution to postural stability. The effect is evident as an initial destabilisation in the sagittal direction and a less transient loss of latero-lateral stability. Running tends to disturb postural stability more than walking, possibly due to more excessive head movement and disturbance of vestibular and visual information centres.

Adult↗

PubMed2001

Glucose, exercise and insulin: emerging concepts.

Physical exercise induces a rapid increase in the rate of glucose uptake in the contracting skeletal muscles. The enhanced membrane glucose transport capacity is caused by a recruitment of glucose transporters (GLUT4) to the sarcolemma and t-tubules. This review summarises the recent progress in the understanding of signals that trigger GLUT4 translocation in contracting muscle. The possible involvement of calcium, protein kinase C (PKC), nitric oxide (NO), glycogen and AMP-activated protein kinase (AMPK) are discussed. Furthermore, the possible mechanisms behind the well-described improvement of insulin action on glucose uptake and glycogen synthase activity in the post-exercise period is discussed. It is concluded that both during and following muscle contractions, glycogen emerges as an important modulator of signalling events in glucose metabolism.

Glucose↗

PubMed2001

Glycogen synthase localization and activity in rat skeletal muscle is strongly dependent on glycogen content.

1. The influence of muscle glycogen content on glycogen synthase (GS) localization and GS activity was investigated in skeletal muscle from male Wistar rats. 2. Two groups of rats were obtained, preconditioned with a combination of exercise and diet to obtain either high (HG) or low (LG) muscle glycogen content. The cellular distribution of GS was studied using subcellular fractionation and confocal microscopy of immunostained single muscle fibres. Stimulation of GS activity in HG and LG muscle was obtained with insulin or contractions in the perfused rat hindlimb model. 3. We demonstrate that GS translocates from a glycogen-enriched membrane fraction to a cytoskeleton fraction when glycogen levels are decreased. Confocal microscopy supports the biochemical observations that the subcellular localization of GS is influenced by muscle glycogen content. GS was not found in the nucleus. 4. Investigation of the effect of glycogen content on GS activity in basal and insulin- and contraction-stimulated muscle shows that glycogen has a strong inhibitory effect on GS activity. Our data demonstrate that glycogen is a more potent regulator of glycogen synthase activity than insulin. Furthermore we show that the contraction-induced increase in GS activity is merely a result of a decrease in muscle glycogen content. 5. In conclusion, the present study shows that GS localization is influenced by muscle glycogen content and that not only basal but also insulin- and contraction-stimulated GS activity is strongly regulated by glycogen content in skeletal muscle.

Animals↗

PubMed2001

Regulation of muscle glucose transport during exercise.

In the present short review some factors affecting glucose utilization during exercise in skeletal muscle will be briefly described. Special focus will be put on the glucose transport step across the sarcolemma. Glucose transporters (GLUT4) are expressed at a surprisingly similar level in the different muscle fiber types in human skeletal muscle in contrast to findings in the rat. When working at the same absolute work load muscle glucose transport is decreased in trained compared with untrained muscle in part due to a decrease in GLUT4 translocation to the sarcolemma in trained muscle. However, when trained and untrained muscle are stressed severely by a workload taxing 100% of their peak oxygen uptake in a glycogen-depleted state, then glucose uptake is larger in trained than in untrained muscle and correlates with muscle GLUT4 content. Finally, the possible role of the AMP-activated protein kinase (AMPK) in regulating glucose uptake during exercise is discussed. It is indicated that at present no experiments definitively link activation of AMPK to activation of muscle glucose transport during exercise.

Biological Transport↗

PubMed2001

Creatine supplementation: exploring the role of the creatine kinase/phosphocreatine system in human muscle.

The effect of oral creatine supplementation on high-intensity exercise performance has been extensively studied over the past ten years and its ergogenic potential in young healthy subjects is now well documented. Recently, research has shifted from performance evaluation towards elucidating the mechanisms underlying enhanced muscle functional capacity after creatine supplementation. In this review, we attempt to summarise recent advances in the understanding of potential mechanisms of action of creatine supplementation at the level of skeletal muscle cells. By increasing intracellular creatine content, oral creatine ingestion conceivably stimulates operation of the creatine kinase (CK)/phosphocreatine (PCr) system, which in turn facilitates muscle relaxation. Furthermore, evidence is accumulating to suggest that creatine supplementation can beneficially impact on muscle protein and glycogen synthesis. Thus, muscle hypertrophy and glycogen supercompensation are candidate factors to explain the ergogenic potential of creatine ingestion. Additional issues discussed in this review are the fibre-type specificity of muscle creatine metabolism, the identification of responders versus non-responders to creatine intake, and the scientific background concerning potential side effects of creatine supplementation.

Creatine↗

PubMed2000

Pro- and macroglycogenolysis in contracting rat skeletal muscle.

Glycogen is present in skeletal muscle in smaller acid-insoluble proglycogen particles and larger acid-soluble macroglycogen particles. The present study was designed to investigate the relative contribution of pro- and macroglycogen to glycogenolysis during muscle contractions. Rats were subjected to a glycogen-depleting exercise bout and refed with either a carbohydrate-rich or fat-rich diet, resulting in widely different muscle glycogen contents. The following day, isolated hindlimbs were perfused and electrically stimulated to contract for 10 min. Pre- and postcontraction muscle samples of soleus, white and red gastrocnemius were analysed for pro- and macroglycogen. Contractions caused significant reductions in both pro- and macroglycogen in all glycogen groups and muscle types. In glycogen-supercompensated gastrocnemius muscles, the relative utilization of macroglycogen was significantly higher than the relative utilization of proglycogen. In muscles with normal to low initial glycogen contents, proglycogen was much more abundant than macroglycogen and therefore contributed more to glycogenolysis in absolute numbers. In conclusion, both proglycogen and macroglycogen are suitable substrates during skeletal muscle contractions, although macroglycogen, when amply available, seems to be more easily broken down. This may provide an explanation for the dependence of the glycogenolytic rate on the total muscle glycogen content.

Animals↗

PubMed2000

Carbohydrate availability affects ammonemia during exercise after beta 2-adrenergic blockade.

PURPOSE: Beta-adrenergic blockade increases blood ammonia concentration during exercise. The purpose of this study was to assess the role of decreased carbohydrate availability in this process. METHODS: Wistar rats (N = 47) were injected intravenously with a selective beta 2-adrenoceptor blocker (ICI 118,551), placebo, or beta 2-blocker + glucose 1 h before a treadmill exercise test. Blood samples were taken to measure the concentration of ammonia, glucose, lactic acid, free fatty acids (FFA), glycerol, branched-chain amino acids (BCAA), and muscle samples for determination of glycogen content. RESULTS: Beta 2-adrenergic blockade shortened running time to exhaustion (23 +/- 4.3 min compared to 44 +/- 5.2 min with placebo), increased blood ammonia levels (146.7 +/- 16.21 micromol x L(-1) compared to 47.5 +/- 0.92 micromol x L(-1) with placebo) and prevented exercise-induced glycogen breakdown in soleus and gastrocnemius muscles. Pre-exercise supplementation of glucose during beta 2-blockade restored exercise-induced glycogen breakdown and reduced blood ammonia concentration during exercise (66.5 +/- 5.65 mmol x L(-1)) but did not improve exercise capacity (26 +/- 3.2 min) when compared with beta2-blockade alone. CONCLUSION: The results suggest that the enhanced rise in blood ammonia concentration during exercise after beta-blockade is caused by impaired carbohydrate availability.

Adrenergic beta-Antagonists↗

PubMed2000

No limiting role for glycogenin in determining maximal attainable glycogen levels in rat skeletal muscle.

We examined whether the protein level and/or activity of glycogenin, the protein core upon which glycogen is synthesized, is limiting for maximal attainable glycogen levels in rat skeletal muscle. Glycogenin activity was 27.5 +/- 1.4, 34.7 +/- 1.7, and 39.7 +/- 1.3 mU/mg protein in white gastrocnemius, red gastrocnemius, and soleus muscles, respectively. A similar fiber type dependency of glycogenin protein levels was seen. Neither glycogenin protein level nor the activity of glycogenin correlated with previously determined maximal attainable glycogen levels, which were 69.3 +/- 5.8, 137.4 +/- 10.1, and 80.0 +/- 5.4 micromol/g wet wt in white gastrocnemius, red gastrocnemius, and soleus muscles, respectively. In additional experiments, rats were exercise trained by swimming, which resulted in a significant increase in the maximal attainable glycogen levels in soleus muscles ( approximately 25%). This increase in maximal glycogen levels was not accompanied by an increase in glycogenin protein level or activity. Furthermore, even in the presence of very high glycogen levels ( approximately 170 micromol/g wet wt), approximately 30% of the total glycogen pool continued to be present as unsaturated glycogen molecules (proglycogen). Therefore, it is concluded that glycogenin plays no limiting role for maximal attainable glycogen levels in rat skeletal muscle.

Animals↗

PubMed2000

Muscle glycogen content affects insulin-stimulated glucose transport and protein kinase B activity.

We investigated the possible regulatory role of glycogen in insulin-stimulated glucose transport and insulin signaling in skeletal muscle. Rats were preconditioned to obtain low (LG), normal, or high (HG) muscle glycogen content, and perfused isolated hindlimbs were exposed to 0, 100, or 10,000 microU/ml insulin. In the fast-twitch white gastrocnemius, insulin-stimulated glucose transport was significantly higher in LG compared with HG. This difference was less pronounced in the mixed-fiber red gastrocnemius and was absent in the slow-twitch soleus. In the white gastrocnemius, insulin activation of insulin receptor tyrosine kinase and phosphoinositide 3-kinase was unaffected by glycogen levels, whereas protein kinase B activity was significantly higher in LG compared with HG. In additional incubation experiments on fast-twitch epitrochlearis muscles, insulin-stimulated cell surface GLUT-4 content was significantly higher in LG compared with HG. The data indicate that, in fast-twitch muscle, the effect of insulin on glucose transport and cell surface GLUT-4 content is modulated by glycogen content, which does not involve initial but possibly more downstream signaling events.

Animals↗

PubMed2000

Dissociation of AMP-activated protein kinase activation and glucose transport in contracting slow-twitch muscle.

5'AMP-activated protein kinase (AMPK) has been suggested to be a key regulatory protein in exercise signaling of muscle glucose transport. To test this hypothesis, we investigated whether muscle glycogen levels affect AMPK activation and glucose transport stimulation similarly during contractions. Rats were preconditioned by a combination of swimming exercise and diet to obtain a glycogen-supercompensated group (high muscle glycogen content [HG]) with approximately 3-fold higher muscle glycogen levels than a glycogen-depleted group (low muscle glycogen content [LG]). In perfused fast-twitch muscles, contractions induced significant increases in AMPK activity and glucose transport and decreases in acetyl-CoA carboxylase (ACC) activity in both HG and LG groups. Contraction-induced glucose transport was nearly 2-fold (P < 0.05) and AMPK activation was 3-fold (P < 0.05) higher in the LG group compared with the HG group, whereas ACC deactivation was not different between groups. Thus, there was a significant positive correlation between AMPK activity and glucose transport in contracting fast-twitch muscles (r = 0.80, P < 0.01). However, in slow-twitch muscles with HG, glucose transport was increased 6-fold (P < 0.05) during contractions, whereas AMPK activity did not increase. In contracting slow-twitch muscles with LG, the increase in AMPK activity (315%) and the decrease in ACC activity (54 vs. 34% at 0.2 mmol/l citrate, LG vs. HG) was higher (P < 0.05) compared with HG muscles, whereas the increase in glucose transport was identical in HG and LG. In conclusion, in slow-twitch muscles, high glycogen levels inhibit contraction-induced AMPK activation without affecting glucose transport. This observation suggests that AMPK activation is not an essential signaling step in glucose transport stimulation in skeletal muscle.

Adenosine Triphosphate↗

PubMed1999

Role of adenosine in regulating glucose uptake during contractions and hypoxia in rat skeletal muscle.

1. The effect of A1-adenosine receptor antagonism via 8-cyclopentyl-1,3-dipropyl-xanthine (CPDPX) on the stimulation of skeletal muscle glucose uptake by contractions and hypoxia was investigated in isolated perfused rat hindquarters. The standard perfusate contained either no insulin or a submaximal insulin concentration at 100 microU ml-1. 2. Muscles were stimulated to contract for 45 min by intermittent tetanic stimulation of the sciatic nerve. Hypoxia was induced by reducing perfusate haematocrit from 30% to 10% on the one hand, and by switching the gassing of the perfusate from a 35% to a 0% O2 mixture for 60 min on the other hand. The effect of contractions and hypoxia alone, or in combination, was investigated. 3. Hypoxia-induced muscle glucose uptake was not altered by CPDPX in the absence or presence of insulin. In contrast, contraction-induced glucose uptake was reduced by approximately 25 % (P < 0.05) by exposure of muscles to CPDPX. CPDPX did not affect hindlimb glucose uptake either before or after contractions. 4. The increment of muscle glucose uptake during hypoxia combined with contractions was greater (P < 0.05) than the effect of hypoxia alone. 5. The current findings provide evidence that the mechanism by which hypoxia stimulates muscle glucose uptake is, at least in part, different from the mechanism of glucose uptake stimulation by contractions, because (i) A1-adenosine receptors regulate insulin-mediated glucose uptake in muscle during contractions but not during hypoxia and (ii) submaximal hypoxia and contractions are additive stimuli to muscle glucose uptake.

Adenosine↗

PubMed1999

Effect of branched-chain amino acids (BCAA), glucose, and glucose plus BCAA on endurance performance in rats.

PURPOSE: The purpose of this study was to assess the effects of pre-exercise administration of branched-chain amino acids (BCAA), glucose, and glucose plus BCAA on time to exhaustion during treadmill exercise in rats. METHODS: Wistar rats were injected intraperitoneally with 1 mL of saline (0.9% NaCl), BCAA (30 mg), glucose (100 mg), or glucose plus BCAA 5 min before either 45 min of submaximal exercise (N = 32) or running to exhaustion (N = 24). After the submaximal exercise test, blood was collected for the measurement of ammonia, BCAA, free tryptophan (free TRP), glucose, free fatty acid, and lactic acid, and muscle samples were taken from the m. soleus for determination of glycogen content. RESULTS: Mean run time to exhaustion was significantly longer after BCAA administration (158+/-26 min) compared with that after saline (118+/-35 min)(P<0.05) but not compared with that after glucose administration (179+/-21 min). When glucose is administered before exercise, the supplementary administration of BCAA had no additional effect on performance (171+/-12 min). The data on blood ammonia, ratio of free TRP/BCAA, and muscle glycogen did not provide a clue for explaining the higher endurance performance after BCAA supplementation. CONCLUSION: The results support the hypothesis that the effect of BCAA administration on performance could be related to carbohydrate availability during exercise.

Amino Acids, Branched-Chain↗

PubMed1999

Contraction-stimulated muscle glucose transport and GLUT-4 surface content are dependent on glycogen content.

The influence of muscle glycogen content on basal and contraction-induced glucose transport and cell surface GLUT-4 content was studied in rat skeletal muscle. Wistar rats were preconditioned by a combination of swimming exercise and diet, resulting in 40% lower (LG) or threefold higher (HG) muscle glycogen content compared with nonexercised controls (NG). At rest and during contractions, 2-deoxy-D-glucose uptake in perfused fast-twitch muscle, but not slow-twitch muscle, was significantly lower in HG compared with LG. Cell surface GLUT-4 content in the fast-twitch plantaris was 994 +/- 180, 1,173 +/- 311, and 2,155 +/- 243 dpm/g in the basal condition and increased (P < 0.05) to 2,285 +/- 239, 3,230 +/- 464, and 4,847 +/- 654 dpm/g during contractions with HG, NG, and LG, respectively, the increase being significantly smaller in HG compared with LG. The contraction-induced increments in glucose transport and in cell surface GLUT-4 content were negatively correlated with the initial glycogen content (P <0.01). In conclusion, glucose transport and cell surface GLUT-4 content in resting and contracting fast-twitch muscle are dependent on the muscle glycogen content.

Animals↗

PubMed1998

Hypoxia and contractions do not utilize the same signaling mechanism in stimulating skeletal muscle glucose transport.

We have investigated whether hypoxia and muscle contractions stimulate glucose transport in perfused rat muscle to the same extent, additively and with the same sensitivity to the microbial products calphostin C and wortmannin. Hindlimb glucose uptake increased gradually from 3.4+/-0.5 to a maximal level of 12.7+/-0.6 micromol g-1 h-1 (n=11) after 50 min of hypoxia. Compared with hypoxia, the effect of maximal electrical stimulation of the sciatic nerve on muscle glucose uptake was more than two-fold higher (27+/-2 micromol g-1 h-1 (n=14)). This was due to a higher contraction- vs. hypoxia-induced glucose transport rate in oxidative fibers. The stimulatory effect of hypoxia and electrical stimulation was not additive. Contraction-induced muscle glucose transport was inhibitable by both calphostin C and wortmannin in the micromolar range, whereas the effect of hypoxia was totally insensitive to these drugs. Our data suggest that diacylglycerol/phorbol ester-sensitive protein kinase C is involved in stimulation of muscle glucose transport by contractions and that in contrast to the prevailing concept, hypoxia and contractions do not stimulate muscle glucose transport by the same signaling mechanism.

Androstadienes↗

PubMed1998

The influence of exercise and dehydration on postural stability.

The aim of this study was to investigate the effects of exercise-induced and thermal dehydration on postural balance. Eight male subjects cycled for 2 h at a power output equal to 57-63% VO2max on two different occasions: once without drinking (NF) and once with intake of 1.9 l of a carbohydrate-electrolyte solution (FR). Before and after the exercise test, the velocity of the centre of pressure (COP) excursion was measured on a force platform during 30-s bipedal standing in normal position, feet side by side, and tandem position, feet heel to toe. On another occasion, eight subjects underwent seven consecutive sauna sessions (85 degrees C, 50% rh) of 15 min duration with no fluid replacement (S) to induce thermal dehydration. Mean fluid loss was 2.7 (+/- 0.4)%, 0.5 (+/- 0.5)% and 3.0 (+/- 0.6)% of body mass after NF, FR and S, respectively. Mean velocity of COP excursion after the exercise test was significantly higher in the NF than in the FR trial (p < 0.05). Postural stability was not influenced by S. In conclusion, prolonged exercise without fluid ingestion seems to negatively affect postural stability, whereas no effect is observed after exercise with fluid replacement or after thermal dehydration.

Adult↗

PubMed1997

Gender differences in blood ammonia response during exercise.

In order to test for possible gender differences in blood ammonia accumulation during exercise, groups of young, physically active women (n = 8) and men (n = 8) performed an incremental load (until exhaustion) and a constant load (30 min at 75% VO2 peak) treadmill exercise test. The groups were matched for physical activity habits. VO2 peak was significantly higher in males (55.8 +/- 2.6 ml/kg/min) than in females (44.5 +/- 2.8 ml/kg/min). During the incremental exercise test to exhaustion blood ammonia concentration progressively increased with increasing workload in both groups. Blood ammonia concentration was significantly higher in males at 70, 80 and 90% of VO2 peak. Peak blood ammonia concentration was higher in males than in females (155 +/- 35 vs 136 +/- 67 mumol/l, respectively), but the difference did not reach the level of statistical significance. During the constant load exercise test blood ammonia concentration increased in both groups. At the end of the exercise test blood ammonia concentration was significantly higher in males than in females (137 +/- 42 vs 91 +/- 24 mumol/l, respectively). In conclusion, the blood ammonia concentration during submaximal exercise is dependent on gender, the males showing higher ammonia concentrations compared to females at the same relative workload (percent of VO2 peak).

Adult↗